Hypokinesia

Decreased movement due to basal ganglia dysfunction

Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinson's disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases. The other category of movement disorder is hyperkinesia that features an exaggeration of unwanted movement, such as twitching or writhing in Huntington's disease or Tourette syndrome.

The most common cause of Hypokinesia is Parkinson's disease, and conditions related to Parkinson's disease. Other conditions may also cause slowness of movements. These include hypothyroidism and severe depression. These conditions need to be carefully ruled out, before a diagnosis of Parkinsonism is made. The remainder of this article describes Hypokinesia associated with Parkinson's disease, and conditions related to Parkinson's disease.

Hypokinetic symptoms arise from damage to the basal ganglia, which plays a role in producing force and computing the effort necessary to make a movement. Two possible neural pathways enable the basal ganglia to produce movement. When activated, the direct pathway sends sensory and motor information from the cerebral cortex to the first structure of the basal ganglia, the putamen. That information directly inhibits the globus pallidus internal and allows free movement. The indirect pathway, traveling through the putamen, globus pallidus external, and subthalamic nucleus, activates the globus pallidus internal threshold and inhibits the thalamus from communicating with the motor cortex, producing hypokinetic symptoms. Recent research indicates, when oscillations fire simultaneously, processing is disrupted at the thalamus and cortex, affecting activities such as motor planning and sequence learning, as well as causing hypokinetic tremors. With increased intake, though, they can become ineffective because of the development of noradrenergic lesions.

Once the reaction to dopaminergic drugs begins to fluctuate in Parkinson's patients, deep brain stimulation (DBS) of the subthalamic nucleus and internal globus pallidus is often used to treat hypokinesia. DBS, like dopaminergic drugs, initially provides relief, but chronic use causes worse hypokinesia and freezing of gait. Lower frequency DBS in irregular patterns has been shown to be more effective and less detrimental in treatment. Patients are usually able to maintain normal levels of fluency, but often stop midsentence, unable to remember or produce a desired word. subjects with faster rates of speech experienced more problems trying to produce conversational language than those who normally spoke at slower rates.

Methylphenidate, commonly used to treat ADHD, has been used in conjunction with levodopa to treat hypokinesia in the short term. Some patients, however, have adverse reactions of nausea and headache to the treatment and the long term effects of the drug treatment still need to be assessed. The successful integration of stem cells can relieve hypokinetic symptoms and decrease the necessary dose of dopaminergic drugs. However, a variety of complications, including possible tumor formation, inappropriate cell migration, rejection of cells by the immune system, and cerebral hemorrhage are possible, causing many physicians to believe the risks outweigh the possible benefits.

Another treatment, still in an experimental stage, is the administration of nociception FQ peptide (NOP) receptor antagonists. This treatment has been shown to reduce hypokinesia in animal studies when increasing nociception FQ in the substantia nigra and subthalamic nucleus. Low doses can be taken with dopaminergic treatment to decrease the amount of L dopa needed, which can reduce its long term side effects and improve motor performance.

Dance therapy has also been shown to reduce hypokinesic movements and rigidity, though targeted more at the muscular aspects of the disorder than the neural activity.

Bradykinesia has been shown to precede impairment of executive functions, working memory, and attention. These cognitive deficiencies can be tied to nonfunction of the basal ganglia and prefrontal cortex, which is also linked to the motor dysfunction of hypokinesia. This suggests that hypokinetic individuals simply have a narrower range of movement that does not increase relative to motivation. Other studies have come to the same conclusion about rewards and hypokinesia, but have shown that aversive stimuli can, in fact, reduce hypokinesic movement. Dopamine is either less involved or has a more complex role in the response to punishment than it does to rewards, as the hypodopaminergic striatum allows more movement in response to aversive stimuli.

Stress causes alterations of cerebral circulation, increasing blood flow in the supramarginal gyrus and angular gyrus of the parietal lobe, the frontal lobe, and the superior temporal gyrus of the left hemisphere. Also, an increase in cardiac activity and change in the tonus of the heart vessels occurs, which is an elementary indication of stress development. In patients with normal stress, an adaptive fight or flight response is usually triggered by sympathetic nervous system activation. Hypokinesia patients experience these typical stress symptoms on a regular basis because of damage to the basal ganglia system. Therefore, when a hypokinesia victim is under stress, he or she does not display a typical fight or flight response, placing the patient under greater danger from potentially harmful stimuli. Low impact exercise, elimination of drug and alcohol use, and regular meditation can help to restore normal stress responses in hypokinesia patients.

Though it is often most associated with Parkinson's disease, hypokinesia can be present in a wide variety of other conditions. Condition Connection to hypokinesia Stroke Damage to certain areas of the brain due to lack of oxygenation has been found to cause hypokinetic symptoms. Frontal and subcortical lesions caused by stroke are more likely to cause hypokinesia than posterior lesions. Schizophrenia The lack of connections between the right supplementary motor area to the pallidum and the left primary motor cortex to the thalamus shown in patients with schizophrenia is thought to lead to hypokinesia. Hyperammonemia Chronic hyperammonemia and liver disease can alter neurotransmission of GABA and glutamate by increasing the amount of glutamate in the substantia nigra and inhibiting movement. Progressive supranuclear palsy Very similar to Parkinson's disease, supranuclear palsy does not actually display the hypokinetic characteristic of progressive loss of movement, despite small amplitude. Diagnosis of hypokinesia can help to distinguish this disorder from Parkinson's.